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C hlamydia trachomatis remodels stable microtubules to coordinate G olgi stack recruitment to the chlamydial inclusion surface
Author(s) -
AlZeer Munir A.,
AlYounes Hesham M.,
Kerr Markus,
AbuLubad Mohammad,
Gonzalez Erik,
Brinkmann Volker,
Meyer Thomas F.
Publication year - 2014
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12829
Subject(s) - microtubule , biology , microbiology and biotechnology , endosome , nocodazole , intracellular , rab , inclusion bodies , cytokinesis , vacuole , intracellular parasite , tubulin , adp ribosylation factor , gtpase , cytoskeleton , cell , biochemistry , cell division , cytoplasm , escherichia coli , endoplasmic reticulum , gene , golgi apparatus
Summary C hlamydia trachomatis ( Ctr ), an obligate intracellular bacterium, survives and replicates within a membrane‐bound vacuole, termed the inclusion, which intercepts host exocytic pathways to acquire nutrients. Ctr subverts cellular trafficking pathways from the G olgi by targeting small GTP ases, including Rab proteins, to sustain intracellular bacterial replication; however, the precise mechanisms involved remain incompletely understood. Here, we show that C hlamydia infection in human epithelial cells induces microtubule remodeling, in particular the formation of detyrosinated stable MTs , to recruit G olgi ministacks, but not recycling endosomes, to the inclusion. These stable microtubules show increased resistance to chemically induced depolymerization, and their selective depletion results in reduced bacterial infectivity. R ab6 knockdown reversibly prevented not only G olgi ministack formation but also detyrosinated microtubule association with the inclusion. Our data demonstrate that C hlamydia co‐opts the function of stable microtubules to support its development.